Gleevec shifts APP processing from a β-cleavage to a nonamyloidogenic cleavage
Abstract
Alzheimer’s disease (AD) is the leading cause of dementia in the elderly. Four approved drugs are used to treat AD cognitive symptoms, including loss of short-term memory. These drugs produce modest, temporary benefits at best and do not prevent or delay worsening of the disease. Recently, a mutation that protects elderly people from developing AD was discovered. The cellular process responsible for the mutation’s protective effect was also identified, suggesting that drugs targeting this process or pathway also might provide protection against the development of AD. In the present study, we discovered that the anticancer drug Gleevec and a related compound mimic the effects of the protective mutation and thus can act as models for the development of effective drugs to fight AD.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jan 23, 2017
- Source ID
- 10.1073/pnas.1620963114
Entities
People
- Karima Bettayeb
- Marc Flajolet
- Paul Greengard
- Subhash C Sinha
- Victor Bustos
- William J. Netzer
Organizations
- The Rockefeller University
- United States Army Medical Research and Development Command